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Big black holes outpace their galaxies in growthhttp://science.psu.edu/news-and-events/2018-news/Brandt2-2018 The growth of the biggest black holes in the universe is outrunning the growth of the galaxies that they inhabit, according to a new study led by researchers at Penn State.

An image from the Chandra Deep Field-South (blue, the deepest ever obtained in X-rays) combined with an optical and infrared image from the Hubble Space Telescope (HST; red, green, and blue). Each Chandra source is produced by hot gas falling towards a supermassive black hole in the center of the host galaxy, as depicted in the artist’s illustration. A new study reveals that, contrary to existing theories, the biggest black holes in the universe do not grow at the same rate as smaller black holes with respect to the growth of the galaxies they inhabit. Credit: NASA/CXC/Penn. State/G. Yang et al and NASA/CXC/ICE/M. Mezcua et al.; Optical: NASA/STScI; Illustration: NASA/CXC/A. Jubett

The growth of the biggest black holes in the universe is outrunning the growth rate of the galaxies that they inhabit, according to a new study led by researchers at Penn State.

For years, astronomers have been studying the formation of galaxies with supermassive black holes -- those with millions to billions of times the mass of the Sun -- at their centers. The prevailing theory suggests that black holes and their host galaxies grow roughly in tandem with each other.

Using data from NASA’s Chandra X-ray Observatory and other telescopes, the new study provides evidence that black holes in massive galaxies have grown much faster than those in less massive ones. The study will appear in the April 2018 issue of the journal Monthly Notices of the Royal Astronomical Society.

“We are trying to reconstruct a race that started billions of years ago,” said Guang Yang, graduate student in astronomy and astrophysics at Penn State and lead author of the study. “We are using extraordinary data taken from different telescopes to figure out how this cosmic competition unfolded.”

Using data from NASA's Chandra X-ray Observatory, the Hubble Space Telescope, and other observatories, Yang and his colleagues studied the growth rate of black holes in galaxies in the distant universe.

“This incredible amount of information, which included data from the Chandra Deep Field-South & North and the COSMOS-Legacy surveys,” said Yang, “allowed us to study the evolution of black holes and their host galaxies starting 12 billion years ago, when the universe was quite young.”

The researchers calculated the ratio between a supermassive black hole's growth rate and the growth rate of its host galaxy. This ratio had been generally thought to be approximately constant for all galaxies. Instead, Yang and colleagues found that this ratio is much higher for more massive galaxies.

"The story appears to be quite different for big and small galaxies," said Fabio Vito, postdoctoral researcher at Penn State and an author of the study. "In big galaxies, the black holes win the race against their hosts. But they lose in small galaxies."

“The black holes in big galaxies grow much faster than would have been expected compared to small galaxies,” said Yang. “For example, if a galaxy is ten times bigger than a second galaxy, then its black hole grows 100 times faster than the second galaxy’s black hole.”

“An obvious question is why,” said Niel Brandt, Verne M. Willaman Professor of Astronomy and Astrophysics and Professor of Physics at Penn State and an author of the paper. “Maybe massive galaxies are more effective at feeding cold gas to their central supermassive black holes than less-massive ones.”

The research team also predicted the accumulated black-hole mass at the current cosmic epoch -- the time we are living now -- by tracking the growth history of black holes.

Their prediction matched direct measurements for big galaxies, suggesting that the team’s predictions successfully recovered the entire cosmic history of black-hole growth.

"Even though the race has been going on for billions of years," said Chien-Ting Chen, postdoctoral researcher at Penn State and another author of the paper, "we can still watch the entire replay with nothing missed."

In addition to Yang, Vito, Brandt, and Chen, the research team at Penn State includes Donald Schneider, Department Head and Distinguished Professor of Astronomy and Astrophysics. The research team also includes Jonathan Trump of the University of Connecticut; Bin Luo of Nanjing University in China; Mouyuan Sun, Yongquan Xue, and Junxian Wang of the University of Science and Technology of China; Anton Koekemoer of the Space Telescope Science Institute; and Christian Vignali of the Università di Bologna in Italy. Many of the additional team members are former graduate students or postdoctoral researchers at Penn State.

This work is supported by the Chandra X-Ray Center, the Penn State ACIS Instrument Team, the National Natural Science Foundation of China, the Ministry of Science and Technology of China, the 973 Program, the CAS Frontier Science Key Research Program, and the Fundamental Research Funds for the Central Universities.

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]]>No publisherglm173astronomy and astrophysicsresearchMain page news2018-02-14T21:18:25Z2018/02/15 11:00:00 US/EasternNews ItemDeep-sea fish use hydrothermal vents to incubate eggshttp://science.psu.edu/news-and-events/2018-news/Fisher2-2018 An international team of researchers, including Penn State biologist Charles Fisher, discovered egg cases of deep-sea fish near hydrothermal vents. The team believes that deep-sea skates use the warm water near the vents to accelerate the typically years-long incubation time of the eggs.

Eggs of deep-sea skates have been discovered near the hottest type of hydrothermal vents, where super-heated water emerges out of the sea floor. These vents, called black smokers, emit dark, sulphurous plumes. Credit: Ocean Exploration Trust

Some deep-sea skates -- cartilaginous fish related to rays and sharks -- use volcanic heat emitted at hydrothermal vents to incubate their eggs, according to a new study in the journal Scientific Reports. Because deep-sea skates have some of the longest egg incubation times, estimated to last more than four years, the researchers believe the fish are using the hot vents to accelerate embryo development. This the first time such behavior has been seen in marine animals.

“Hydrothermal vents are extreme environments, and most animals that live there are highly evolved to live in this environment,” said Charles Fisher, Professor and Distinguished Senior Scholar of Biology at Penn State and an author of the paper. “This study is one of the few that demonstrates a direct link between the vent environment and animals that live most of their life elsewhere.”

Among the least explored and unique ecosystems, deep-sea hydrothermal fields are regions on the sea floor where hot water emerges after being heated in the ocean crust. In their study, an international team of researchers used a remotely operated underwater vehicle (ROV) to survey in and around an active hydrothermal field located in the Galápagos archipelago, 28 miles north of Darwin Island.

Over 150 egg cases were discovered near a black smoker in the deep waters near the Galápagos Islands. The research team collected four egg cases using a remotely operated underwater vehicle for DNA analysis. Credit: Ocean Exploration Trust

“The first place the ROV landed on the sea floor was on a ridge, in the plume of a nearby hydrothermal vent that we had specifically come to investigate – a black smoker,” said Fisher. “When we panned the camera down, we found something we did not expect: These giant egg cases, also known as mermaid purses. And we found several layers of them, indicating that whatever was laying these eggs had been coming back to this spot for many years to lay them. As the dive progressed, we saw more and more of these egg cases and realized that this was not the result of a single animal, but rather a behavior shared by many individuals."

The researchers found 157 egg cases in the area and collected four with the ROV’s robotic arm. DNA analysis revealed that the egg cases belonged to the skate species Bathyraja spinosissima, one of the deepest-living species of skates that is not typically thought to occur near the vents. The majority -- 58 percent -- of the observed egg cases were found within about 65 feet of the chimney-like black smokers, the hottest kind of hydrothermal vents, and over 89 percent had been laid in places where the water was hotter than average. The researchers believe that the warmer temperatures in the area could reduce the typically years-long incubation time of the eggs.

While several species of reptiles and birds lay their eggs in locations that optimize soil temperatures, only two other groups of animals are known to use volcanically heated soils: the modern-day Polynesian megapode -- a rare bird native to Tonga -- and a group of nest-building neosauropod dinosaurs from the Cretaceous Period.

Video credit: Ocean Exploration Trust, Penn State

Because of their long lifespan and slow rate of development, deep-water skates may be particularly sensitive to threats to their environment, including fisheries expanding into deeper waters and sea-floor mining. Understanding the development and habitat of the skates is vital for developing effective conservation strategies for this poorly understood species.

DNA analysis revealed that the egg cases found near the black smoker belong to the skate species Bathyraja spinosissima, commonly known as deep-sea skates. The researchers believe the fish use the volcanic heat emitted from the hydrothermal vents to accelerate the typically years-long incubation time of the eggs. Credit: Julye Newlin, Ocean Exploration Trust

“The deep sea is full of surprises,” said Fisher. “I've made hundreds of dives, both in person and virtually, to deep sea hydrothermal vents and have never seen anything like this.”

In addition to Fisher, the research team includes Pelayo Salinas-de-León and Florencia Cerutti-Pereyra of the Charles Darwin Research Station in Ecuador and the National Geographic Society; Brennan Philips of Harvard University and the University of Rhode Island; David Ebert of the Moss Landing Marine Laboratories, California Academy of Sciences and the South African Institute for Aquatic Biodiversity; Mahmood Shivji and Cassandra Ruck of Nova Southeastern University; and Leigh Marsh of University of Southampton, Waterfront Campus, and the National Oceanography Centre, both in the United Kingdom. This work was funded by the National Oceanic and Atmospheric Administration (NOAA), the Helmsley Charitable Trust, and the Save Our Seas Foundation.

[ Gail McCormick / Nature Research ]

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]]>No publisherglm173biologyresearchMain page news2018-02-12T14:38:55Z2018/02/12 10:15:00 US/EasternNews ItemNew neuron-like cells allow investigation into synthesis of vital cellular componentshttp://science.psu.edu/news-and-events/2018-news/Szpara1-2018 Using a new method to create synthetic neurons, a team of researchers from Penn State explores how the human brain makes a metabolic building block essential for the survival of all living organisms. The team describes a core enzyme involved in the synthesis of these building blocks, called purines, and how the enzyme might change during infection by herpes simplex virus.

The enzyme called FGAMS (red) is expressed in human neuron-like cells, which suggests its involvement in the synthesis of purines, a component of DNA involved in many other cellular and metabolic processes. Using a new method to create synthetic neurons from a readily available cell line, a new study explores the role of FGAMS in creating a multi-enzyme complex called the purinosome, which enables faster production of purines. Credit: Colleen Mangold, Penn State

Neuron-like cells created from a readily available cell line have allowed researchers to investigate how the human brain makes a metabolic building block essential for the survival of all living organisms. A team led by researchers from Penn State optimized a new method to create the synthetic neurons, which they used to investigate a core enzyme involved in the synthesis of purines -- a component of DNA that is involved in many other cellular and metabolic processes -- and how the enzyme might change during infection by herpes simplex virus. An early version of the paper describing the enzyme appears online in January 2018 in the Journal of Neurochemistry, and a paper describing the neuron-like cells appeared in the December 2017 issue of the Journal of Virology.

“These newly developed neuron-like cells allowed us to investigate purine formation in a specialized cell type for the first time,” said Moriah Szpara, assistant professor of biochemistry and molecular biology at Penn State and senior author of both papers. “We were interested in neurons because they require a lot of energy and therefore need to produce purines efficiently. We were also curious how the synthesis process might be affected by infection with herpes simplex virus, an energetically demanding virus that takes up residence in neurons.”

When demand for purines is high in a cell, a complex composed of many enzymes called the purinosome forms to enable faster production of these important chemicals. The researchers investigated an enzyme called FGAMS, a core component of the purinosome. To better understand the role of FGAMS in purine production, they looked at where and how much of the enzyme is expressed in rodent brain slices, rodent neurons, human non-neuronal cells, and the human neuron-like cells cultivated with the new technique.

“Studying human neurons has been challenging because we haven’t had a good laboratory model to study them,” said Colleen Mangold, a postdoctoral researcher at Penn State and an author of both studies. “We can use neurons from rodents or chick embryos, but they don’t give us the same information as human cells. Most studies require large numbers of cells, so we developed a method to take a commonly available cell line and shape it into cells that look and act like neurons. This new method will allow us to start asking the backlog of questions we have about neurons, like how purines are synthesized in the brain.”

In the neuron-like cells and in rodent neurons and brain slices, FGAMS was expressed in a number of locations throughout the neuron, including near mitochondria and microtubules. Because FGAMS is also found near these structures in non-neuronal cells, the researchers suspect that purinosome formation may be conserved across different cell types.

The researchers also investigated the effect of infection with herpes simplex virus 1 (HSV1) on the purine biosynthesis protein FGAMS both in neurons and in non-neuronal cells. HSV1 initially infects an individual at the skin surface and proceeds to set up a lifelong infection in neurons that cannot be cleared by the immune system. Because purines may play a role in the replication of HSV1, the high metabolic load of the virus might deplete purine resources and affect purine synthesis.

“Infection with HSV1 induced clustering of FGAMS in the non-neuronal cells, which model the skin phase of infection, while FGAMS appeared to be constantly clustered and activated in neuronal cells,” said Stephen Benkovic, Evan Pugh Professor of Chemistry and Holder of the Eberly Family Chair in Chemistry at Penn State and an author of the purine formation paper. “We suspect that the purinosome is assembled only on an as-needed basis in non-neuronal cells, but that high energetic demands in neurons may necessitate the purinosome being present all of the time.”

“Viruses like HSV1 survive by establishing a lifelong infection in neurons,” said Szpara, “and there is growing evidence suggesting links between chronic viral infections and late-life neurocognitive diseases. We are continuing to investigate the potential connections between the burdens of viral infection and the high metabolic demands of neurons to see if there are avenues to prevent damage and improve long-term neuronal health.”

Because the results from the neuron-like cells mirror those in the rodent brain slices and neurons, this study highlights the utility of these cells as a new model system for studying neurons and how viruses affect them.

“These neuron-like cells are easy to grow in great numbers and will allow us to capture some of the nuance we missed when studying viruses in non-neuronal cells,” said Mackenzie Shipley, graduate student at Penn State and first author of the synthetic neuron paper. “While these cells can be used to ask a variety of questions about neurons, they also provide a new avenue to study how neurons respond to neurotropic viruses, like HSV, HIV, rabies, West Nile, Zika, and Chikungunya.”

In addition to Szpara, Mangold, and Benkovic, the research team on the project exploring the formation of purines includes Pamela Yao of the National Institutes of Health (NIH) National Institute of Aging, and Mei Du and Willard Freeman of the University of Oklahoma Health Sciences Center. This work is funded in part by NIH, the American Heart Association, the NIH National Institute of Aging, the Huck Institutes of the Life Sciences at Penn State, and the Pennsylvania Department of Health Commonwealth Universal Research Enhancement (CURE) program.

In addition to Szpara, Mangold, and Shipley, the research team on the project describing the neuron-like cells includes Chad Kuny, postdoctoral researcher at Penn State. This work is funded by the NIH National Institute of Allergy and Infectious Diseases (NAID) Virus Pathogens Resource (ViPR) Bioinformatics Resource Center, and is supported by the Huck Institutes of the Life Sciences.

One of the biggest mysteries in astroparticle physics has been the origins of ultrahigh-energy cosmic rays, very high-energy neutrinos, and high-energy gamma rays. Now, a new theoretical model reveals that they all could be shot out into space after cosmic rays are accelerated by powerful jets from supermassive black holes and they travel inside clusters and groups of galaxies.

The model explains the natural origins of all three types of "cosmic messenger" particles simultaneously, and is the first astrophysical model of its kind based on detailed numerical computations. A scientific paper that describes this model, produced by Penn State and University of Maryland scientists, will be published as an Advance Online Publication on the website of the journal Nature Physics on January 22, 2018.

"Our model shows a way to understand why these three types of cosmic messenger particles have a surprisingly similar amount of power input into the universe, despite the fact that they are observed by space-based and ground-based detectors over ten orders of magnitude in individual particle energy," said Kohta Murase, assistant professor of physics and astronomy and astrophysics at Penn State. "The fact that the measured intensities of very high-energy neutrinos, ultrahigh-energy cosmic rays, and high-energy gamma rays are roughly comparable tempted us to wonder if these extremely energetic particles have some physical connections. The new model suggests that very high-energy neutrinos and high-energy gamma rays are naturally produced via particle collisions as daughter particles of cosmic rays, and thus can inherit the comparable energy budget of their parent particles. It demonstrates that the similar energetics of the three cosmic messengers may not be a mere coincidence."

Ultrahigh-energy cosmic rays are the most energetic particles in the universe -- each of them carries an energy that is too high to be produced even by the Large Hadron Collider, the most powerful particle accelerator in the world. Neutrinos are mysterious and ghostly particles that hardly ever interact with matter. Very high-energy neutrinos, with energy more than one million mega-electronvolts, have been detected in the IceCube neutrino observatory in Antarctica. Gamma rays have the highest-known electromagnetic energy -- those with energies more than a billion times higher than a photon of visible light have been observed by the Fermi Gamma-ray Space Telescope and other ground-based observatories. "Combining all information on these three types of cosmic messengers is complementary and relevant, and such a multi-messenger approach has become extremely powerful in the recent years," Murase said.

Murase and the first author of this new paper, Ke Fang, a postdoctoral associate at the University of Maryland, attempt to explain the latest multi-messenger data from very high-energy neutrinos, ultrahigh-energy cosmic rays, and high-energy gamma rays, based on a single but realistic astrophysical setup. They found that the multi-messenger data can be explained well by using numerical simulations to analyze the fate of these charged particles.

"In our model, cosmic rays accelerated by powerful jets of active galactic nuclei escape through the radio lobes that are often found at the end of the jets," Fang said. "Then we compute the cosmic-ray propagation and interaction inside galaxy clusters and groups in the presence of their environmental magnetic field. We further simulate the cosmic-ray propagation and interaction in the intergalactic magnetic fields between the source and the Earth. Finally we integrate the contributions from all sources in the universe."

The leading suspects in the half-century old mystery of the origin of the highest-energy cosmic particles in the universe were in galaxies called "active galactic nuclei," which have a super-radiating core region around the central supermassive black hole. Some active galactic nuclei are accompanied by powerful relativistic jets. High-energy cosmic particles that are generated by the jets or their environments are shot out into space almost as fast as the speed of light.

"Our work demonstrates that the ultrahigh-energy cosmic rays escaping from active galactic nuclei and their environments such as galaxy clusters and groups can explain the ultrahigh-energy cosmic-ray spectrum and composition. It also can account for some of the unexplained phenomena discovered by ground-based experiments," Fang said. "Simultaneously, the very high-energy neutrino spectrum above one hundred million mega-electronvolts can be explained by particle collisions between cosmic rays and the gas in galaxy clusters and groups. Also, the associated gamma-ray emission coming from the galaxy clusters and intergalactic space matches the unexplained part of the diffuse high-energy gamma-ray background that is not associated with one particular type of active galactic nucleus."

"This model paves a way to further attempts to establish a grand-unified model of how all three of these cosmic messengers are physically connected to each other by the same class of astrophysical sources and the common mechanisms of high-energy neutrino and gamma-ray production," Murase said. "However, there also are other possibilities, and several new mysteries need to be explained, including the neutrino data in the ten-million mega-electronvolt range recorded by the IceCube neutrino observatory in Antarctica. Therefore, further investigations based on multi-messenger approaches -- combining theory with all three messenger data -- are crucial to test our model."

The new model is expected to motivate studies of galaxy clusters and groups, as well as the development of other unified models of high-energy cosmic particles. It is expected to be tested rigorously when observations begin to be made with next-generation neutrino detectors such as IceCube-Gen2 and KM3Net, and the next-generation gamma-ray telescope, Cherenkov Telescope Array.

"The golden era of multi-messenger particle astrophysics started very recently," Murase said. "Now, all information we can learn from all different types of cosmic messengers is important for revealing new knowledge about the physics of extreme-energy cosmic particles and a deeper understanding about our universe."

The research was partially supported by the National Science Foundation (grant No. PHY-1620777) and the Alfred P. Sloan Foundation.

The 48-hour lifecycle of Plasmodium falciparum development in human red blood cells. A team of researchers has used whole genome analysis and chemogenetics to identify new drug targets and resistance genes in the parasite. Credit: Llinás Laboratory, Penn State

Researchers at University of California San Diego School of Medicine and Penn State, with a consortium of colleagues across the country and around the world, have used whole genome analyses and chemogenetics to identify new drug targets and resistance genes in 262 parasite cell lines of Plasmodium falciparum – the protozoan pathogen that cause malaria – that are resistant to 37 diverse antimalarial compounds.

The study, published in the January 12, 2018 issue of Science, confirmed previously known genetic modifications that substantially contribute to the parasites’ drug resistance, but also revealed new targets that deepen understanding of the parasites’ underlying biology.

“This exploration of the P. falciparum resistome – the collection of antibiotic resistance genes – and its druggable genome will help guide new drug discovery efforts and advance our understanding of how the malaria parasite evolves to fight back,” said senior author Elizabeth Winzeler, professor of pharmacology and drug discovery in the Department of Pediatrics at UC San Diego School of Medicine.

P. falciparum is a unicellular protozoan transmitted to humans through the bite of infected Anopheles mosquitos. It is responsible for approximately half of all malaria cases. Malaria’s massively disproportionate impact on human health – the World Health Organization estimates there were 216 million cases worldwide and 445,000 deaths in 2016 – is due in part to the parasites’ particular adeptness at changing genomes to evade and resist drug treatment and the human immune system.

“A single human infection can result in a person containing upwards of a trillion asexual blood stage parasites,” said Winzeler. “Even with a relatively slow random mutation rate, these numbers confer extraordinary adaptability. In just a few cycles of replication, the P. falciparum genome can acquire a random genetic change that may render at least one parasite resistant to the activity of a drug or human-encoded antibody.”

Such rapid evolution poses significant challenges to controlling the disease, said researchers, but it can also be exploited in laboratory studies to document precisely how the parasite evolves in the presence of known antimalarials to create drug resistance. It can also be used to reveal new drug targets.

Rather than focus on the interaction of parasites with single antimalarial compounds or investigate single suspect genes in P. falciparum, Winzeler and colleagues used whole genome sequencing and tested a diverse set of antimalarial compounds. The resulting dataset revealed a large range of mutations in the parasite that arose during selection under drug pressure. Resistant parasites often contained a mutation in a presumptive drug-target gene and additional mutations in other, unrelated genes.

“Our findings showed and underscored the challenging complexity of evolved drug resistance in P. falciparum,” said Winzeler, “but they also identified new drug targets or resistance genes for every compound for which resistant parasites were generated. It revealed the complicated chemogenetic landscape of P. falciparum, but also provided a potential guide for designing new small molecule inhibitors to fight this pathogen.”

To functionally validate the modes of action for the antimalarial compounds and their association with the predicted target genes, Manuel Llinás, professor of biochemistry and molecular biology at Penn State, and members of his lab used mass spectrometry-based metabolomics to assess the chemical fingerprints induced in the parasites upon drug exposure.

“These results provide a key link to understanding how malaria parasites respond metabolically to drug pressure in the short term,” said Llinás, “and they also allow us to connect how this pressure is relieved through genomic mutations that lead to resistance in the parasites. This knowledge could aid in the design of future antimalarial drugs that may slow the development of resistance.”

Funding support for this research came, in part, from the Bill and Melinda Gates Foundation, the U.S. National Institutes of Health, the U.S. National Institute of Allergy and Infectious Diseases, a UC San Diego Division of Infectious Diseases institutional NIAID training grant, a NIAID NRSA fellowship, the U.S. National Institute of General Medical Sciences, and an A.P. Giannini Post-Doctoral Fellowship.

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]]>No publishersjs144biochemistry and molecular biologyresearchMain page news2018-01-18T22:56:46Z2018/01/11 14:05:00 US/EasternNews ItemHave RNA, will travel: Malaria parasite packs genetic material in preparation for trip from mosquitoes to humanshttp://science.psu.edu/news-and-events/2018-news/Lindner1-2018 The parasite that causes malaria has not one, but two, specialized proteins that protect its genetic material until the parasite takes up residence in a new host.

Because the malaria parasite Plasmodium cannot anticipate when it may be transmitted from a mosquito to a mammalian host, it uses specialized poly(A)-binding proteins to package and protect its genetic material for use after transmission. Credit: Centers for Disease Control and Prevention

The parasite that causes malaria has not one, but two, specialized proteins that protect its messenger RNAs -- genetic material that encodes for proteins -- until the parasite takes up residence in a new mosquito or a human host. A new study by researchers at Penn State describes the two proteins and reveals an additional role that one may play to facilitate RNA-based interactions between the parasite, its mosquito vector, and its human host. The study appears January 10, 2018, in the journal mSphere.

“Understanding the malaria parasite and how it interacts with its host may provide insights that could help prevent the spread of this often-fatal disease,” said Scott Lindner, assistant professor of biochemistry and molecular biology at Penn State and senior author of the study. “The malaria parasite has a complex life cycle that includes phases in the mosquito vector, the human liver, and in human blood. Moreover, the parasite has no idea when it’s going to be transmitted from a mosquito to a human host and back, so it always needs to be ready to be transmitted. It prepares for this by making and packaging up the mRNAs that it will eventually need for making proteins inside its new host or a new mosquito.”

During this process, called translational repression, special proteins bind to mRNAs and prevent them from being translated into protein. One protein involved binds to the mRNA’s poly(A) tail -- a repeated string of As or adenosine molecules added to the end of most mRNA strands. This helps to form a complex of proteins and RNA that is silenced but poised for action after the parasite is transmitted to the host. Most single-celled organisms have one type of this poly(A)-binding protein, while multi-cellular organisms have two. In this study, the researchers characterize two types of poly(A)-binding proteins in the single-celled Plasmodium parasite, both of which contribute to translational regulation.

“We knew from our lab’s previous work that Plasmodium had a type of poly(A)-binding protein that functions outside of the nucleus of the cell,” said Allen Minns, research technician at Penn State and first author of the paper. “This protein binds and protects the poly(A) tail at one end of an mRNA strand. In this study, we used biochemical approaches to further characterize this protein, and found that it also has a specialized job receiving mRNAs. It forms chains without the presence of RNA, which potentially allows large assemblies of the protein to quickly protect the entire length of the poly(A) tail.”

The malaria sporozoite, tagged with fluorescent dye in this image, contains the non-nuclear form of a poly(A)-binding protein on its surface. The unexpected role of this protein on the infectious form of the malaria parasite is not yet clear but may provide an opportunity for the parasite to interact with its mosquito vector or its human host through RNA. Credit: Penn State

The researchers also identified and characterized a second type of poly(A)-binding protein that functions inside the nucleus of the parasite during the blood stages of its life cycle. In multi-cellular organisms, this second poly(A)-binding protein usually performs a quality control check before mRNA exits the nucleus, confirming that the mRNA is constructed properly. These quality control proteins then pass on the mRNA strand to other proteins outside of the nucleus, which direct the mRNA to be translated or to be packaged for later use through translational repression.

In addition to an important role in translational regulation inside of the cell, the researchers also discovered that the non-nuclear poly(A)-binding protein may play a surprising role outside of the cell.

“When the parasite takes the form of a sporozoite in the mosquito, we actually don’t see the vast majority of the non-nuclear poly(A)-binding protein inside the cell where we expected it to be -- where it would interact with mRNAs produced by the parasite,” said Lindner. “Instead, the protein accumulates at the surface of the sporozoite and is shed when the parasite moves. We don’t see this happening in other life stages of the parasite, and this is now the third RNA-binding protein found to be on the surface of the sporozoite. The parasite is putting these RNA-binding proteins out there on its surface for a reason; the new and exciting question is why.”

The researchers speculate that the poly(A)-binding proteins on the sporozoite surface allow the parasite to interact with RNA from sources outside of the parasite and could thus provide an opportunity for the parasite to interact with the mosquito or the host through their RNA.

“This study suggests that the parasite’s interaction with outside RNA is probably much more pervasive than we thought it was,” said Lindner. “It is possible that this kind of interaction could eventually provide a new target for intervention strategies, but the first step is understanding why the malaria parasite has these poly(A)-binding proteins on the sporozoite surface.”

In addition to Lindner and Minns, the research team includes Penn State graduate students Kevin Hart and Suriyasri Subramanian, and Susan Hafenstein, associate professor of biochemistry and molecular biology at Penn State University Park and associate professor medicine and of microbiology and immunology at the Penn State College of Medicine. This work was funded by the National Institutes of Health and supported by the Huck Institutes of the Life Sciences.

[Gail McCormick]

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]]>No publisherglm173biochemistry and molecular biologyresearchMain page news2018-01-11T15:14:45Z2018/01/10 15:35:00 US/EasternNews ItemHow massive is supermassive? Astronomers measure more black holes, farther awayhttp://science.psu.edu/news-and-events/2018-news/Grier1-2018 A team of astronomers from the Sloan Digital Sky Survey (SDSS), including several Penn State scientists, announced new measurements of the masses of a large sample of supermassive black holes far beyond the local universe.

An artist's rendering of the inner regions of an active galaxy/quasar, with a supermassive black hole at the center surrounded by a disk of hot material falling in. The inset at the bottom right shows how the brightness of light coming from the two different regions changes with time. The time span covered by these two light curves is about six months. The bottom plot echoes the top, with a slight time delay of about 10 days indicated by the vertical line. This means that the distance between these two regions is about 10 light-days (about 150 billion miles, or 240 million kilometers). Credit: Nahks Tr'Ehnl (www.nahks.com) and Catherine Grier (Penn State) and the SDSS collaboration

A team of astronomers from the Sloan Digital Sky Survey (SDSS), including several Penn State scientists, announced new measurements of the masses of a large sample of supermassive black holes far beyond the local universe.

The results, being presented at the American Astronomical Society (AAS) meeting in National Harbor, Maryland and published in the Astrophysical Journal, represent a major step forward in our ability to measure supermassive black hole masses in large numbers of distant quasars and galaxies.

"This is the first time that we have directly measured masses for so many supermassive black holes so far away," said Catherine Grier, a postdoctoral fellow at Penn State and the lead author of this work. "These new measurements, and future measurements like them, will provide vital information for people studying how galaxies grow and evolve throughout cosmic time."

Supermassive black holes are found in the centers of nearly every large galaxy, including those in the farthest reaches of the universe. Their gravitational pull is so great that nearby dust and gas is inexorably drawn in. The infalling material heats up to such high temperatures that it glows brightly enough to be seen all the way across the universe, forming bright disks of hot gas known as quasars. By studying quasars, we learn not only about super massive black holes, but also about the distant galaxies that they live in. But to do all of this requires measurements of the properties of the supermassive black holes, most importantly their masses.

“The problem is that measuring the masses of super massive black holes is a daunting task,” said Grier. “Astronomers measure supermassive black hole masses in nearby galaxies by observing groups of stars and gas near the galaxy center. However, these techniques do not work for more distant galaxies, because they are so far away that telescopes cannot resolve their centers.”

A graph of known supermassive black hole masses at various lookback times, which measures the time into the past we see when we look at each quasar. More distant quasars have longer lookback times (since their light takes longer to travel to Earth), so we see them as they appeared in the more distant past. The universe is about 13.8 billion years old, so the graph goes back to when the universe was about half of its current age. The black hole masses measured in this work are shown as purple circles, while gray squares show black hole masses measured by prior reverberation mapping projects. The sizes of the squares and circles are related to the masses of the black holes they represent. The graph shows black holes from 5 million to 1.7 billion times the mass of the Sun. Credit: Catherine Grier (Penn State) and the SDSS collaboration

Instead, direct mass measurements of supermassive black holes in galaxies farther away are made using a technique called reverberation mapping. Reverberation mapping works by comparing the brightness of light coming from gas very close in to the black hole to the brightness of light coming from fast-moving gas farther out. Changes occurring in the inner region impact the outer region, but light takes time to travel outwards, or "reverberate." This reverberation means that there is a time delay between the variations seen in the two regions. By measuring this time delay, astronomers can determine how far out the gas is from the black hole. Knowing that distance allows them to measure the mass of the supermassive black hole -- even though they can't see the details of the black hole itself.

Over the past 20 years, astronomers have used reverberation mapping to laboriously measure the masses of around 60 supermassive black holes in nearby active galaxies. But because each measurement requires months of observation, measurements are typically made for only a handful of active galaxies at a time. Using reverberation mapping on quasars, which are farther away, is even more difficult, requiring years of repeated observations. Because of these observational difficulties, astronomers had only successfully used the technique to measure supermassive black hole masses for a handful of more distant quasars -- until now.

In this new work, Grier's team has used an industrial-scale application of reverberation mapping with the goal of measuring black hole masses in tens to hundreds of quasars. The key to the success of the SDSS Reverberation Mapping project lies in the SDSS's ability to study many quasars at once -- the program is currently observing about 850 quasars simultaneously. But even with the SDSS's powerful telescope, this is a challenging task because these distant quasars are incredibly faint.

"You have to calibrate these measurements very carefully to make sure you really understand what the quasar system is doing," said Jon Trump, assistant professor at the University of Connecticut (previously a Hubble Postdoctoral Fellow at Penn State) and a member of the research team.

Improvements in the calibrations were obtained by also observing the quasars with the Canada-France-Hawaii-Telescope (CFHT) and the Steward Observatory Bok telescope located at Kitt Peak over the same observing season. After all of the observations were compiled and the calibration process was completed, the team found reverberation time delays for 44 quasars. They used these time delay measurements to calculate black hole masses that range from about 5 million to 1.7 billion times the mass of our Sun.

"This is a big step forward for quasar science," said Aaron Barth, a professor of astronomy at the University of California, Irvine who was not involved in the team’s research. "They have shown for the first time that these difficult measurements can be done in mass-production mode."

These new SDSS measurements increase the total number of active galaxies with supermassive black hole mass measurements by about two-thirds, and push the measurements farther back in time to when the universe was only half of its current age. But the team isn't stopping there -- they continue to observe these 850 quasars with SDSS, and the additional years of data will allow them to measure black hole masses in even more distant quasars, which have longer time delays that cannot be measured with a single year of data.

"Getting observations of quasars over multiple years is crucial to obtain good measurements," says Yue Shen, an assistant professor at the University of Illinois and principal investigator for the project. "As we continue our project to monitor more and more quasars for years to come, we will be able to better understand how supermassive black holes grow and evolve."

The future of the SDSS holds many more exciting possibilities for using reverberation mapping to measure masses of supermassive black holes across the universe. After the current fourth phase of the SDSS ends in 2020, the fifth phase of the program, SDSS-V, begins. SDSS-V features a new program called the Black Hole Mapper, which plans to measure supermassive black hole masses in more than 1,000 more quasars, pushing farther out into the universe than any reverberation mapping project ever before.

"The Black Hole Mapper will let us move into the age of supermassive black hole reverberation mapping on a true industrial scale," said Niel Brandt, professor of astronomy and astrophysics at Penn State and a long-time member of the SDSS. "We will learn more about these mysterious objects than ever before."

In addition to Grier and Brandt, the SDSS Reverberation Mapping project team at Penn State includes Distinguished Professor of Astronomy and Astrophysics Donald P. Schneider.

ABOUT THIS RESEARCH

This research was supported by funding from the U.S. National Science Foundation (NSF) and the Penn State Willaman Endowment. The SDSS-RM team would also like to acknowledge support from the Alfred P. Sloan Research Fellowship, the NSF, the U.K. Science and Technology Facilities Council, the National Key R&D Program of China, and the National Science Foundation of China.

This work is also based on observations obtained with MegaPrime/MegaCam, a joint project of CFHT and CEA/DAPNIA, at the Canada-France–Hawaii Telescope (CFHT), which is operated by the National Research Council (NRC) of Canada, the Institut National des Sciences de l'Univers of the Centre National de la Recherche Scientifique of France, and the University of Hawaii.

ABOUT THE SLOAN DIGITAL SKY SURVEY

Funding for the Sloan Digital Sky Survey IV has been provided by the Alfred P. Sloan Foundation, the U.S. Department of Energy Office of Science, and the Participating Institutions. SDSS acknowledges support and resources from the Center for High-Performance Computing at the University of Utah. The SDSS web site is www.sdss.org.

SDSS is managed by the Astrophysical Research Consortium for the Participating Institutions of the SDSS Collaboration including the Brazilian Participation Group, the Carnegie Institution for Science, Carnegie Mellon University, the Chilean Participation Group, the French Participation Group, Harvard-Smithsonian Center for Astrophysics, Instituto de Astrofísica de Canarias, The Johns Hopkins University, Kavli Institute for the Physics and Mathematics of the Universe (IPMU) / University of Tokyo, Lawrence Berkeley National Laboratory, Leibniz Institut für Astrophysik Potsdam (AIP), Max-Planck-Institut für Astronomie (MPIA Heidelberg), Max-Planck-Institut für Astrophysik (MPA Garching), Max-Planck-Institut für Extraterrestrische Physik (MPE), National Astronomical Observatories of China, New Mexico State University, New York University, University of Notre Dame, Observatório Nacional / MCTI, The Ohio State University, Pennsylvania State University, Shanghai Astronomical Observatory, United Kingdom Participation Group, Universidad Nacional Autónoma de México, University of Arizona, University of Colorado Boulder, University of Oxford, University of Portsmouth, University of Utah, University of Virginia, University of Washington, University of Wisconsin, Vanderbilt University, and Yale University.

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]]>No publishersjs144astronomy and astrophysicsresearchsdssMain page news2018-01-17T15:55:39Z2018/01/10 15:20:00 US/EasternNews ItemNew research agenda for malaria elimination and eradicationhttp://science.psu.edu/news-and-events/2018-news/Llinas1-2018 Manuel Llinás, professor of biochemistry and molecular biology, and Jason Rasgon, professor of entomology and disease epidemiology, have participated in the formulation of an updated research agenda for global malaria elimination and eradication.

Two Penn State researchers have participated in the formulation of a new updated research agenda for global malaria elimination and eradication. Together with more than 180 scientists, malaria program leaders, and policy makers from around the world, Manuel Llinás, professor of biochemistry and molecular biology, and Jason Rasgon, professor of entomology and disease epidemiology, contributed to the Malaria Eradication Research Agenda (malERA) Refresh Collection, which defines a forward-looking research and development agenda that will accelerate progress towards malaria elimination and global eradication. The malERA Refresh collaboration resulted in seven research papers that were recently published as a special collection in the journal PLOS Medicine.

A world free of malaria would present enormous benefits in terms of health, equity and economy. The World Health Organization has set ambitious goals for reducing the burden of malaria, and 21 countries have been identified as having the potential to eliminate local transmission of malaria by 2020. However, there is no easy path to achieving a malaria-free world, and there is a real need for innovation. The malERA Refresh lays out a research agenda to meet the challenges and, in the long-term eradicate malaria globally.

“The malERA Refresh allowed the community of malaria experts to re-examine its priorities,” said Llinás. “It provides ideas and suggestions that will impact everything from basic science to policy to the roll out of new drugs.”

The initial malERA agenda from 2011 aimed to identify key knowledge gaps and define the strategies and tools that could lead to the elimination and eradication of malaria. To update the agenda, six panels with malaria experts from around the world engaged in a collaborative process to address progress made and identify the main challenges across the following areas: basic science and enabling technologies; combination interventions and modeling; diagnostics, drugs, vaccines and vector control; insecticide and drug resistance; characterizing the reservoir and measuring transmission; and health systems and policy research.

"The malERA papers provide a framework for focus for research funders whether government or private; for the World Health Organization, where recommendations on tools and strategies are made; and for each country, which has to make the specific decisions to shape its programs,” said Regina Rabinovich, chair of the Malaria Eradication Scientific Alliance (MESA), which coordinated the collaboration. “The global malaria enterprise remains hugely challenging, and transforming the mindset from implementation to problem solving is an essential task for both the next generation of scientists and program implementers."

Llinás contributed to the panel regarding basic science and how it enables new drug interventions. In the resulting paper, the panel identified future research opportunities to better understand the life cycle of the malaria-causing Plasmodium parasite and address unanswered questions about transmission.

“The best way to answer these questions is by combining forces,” said Llinás, “using tools from human immunology, parasitology, and entomology, and by taking advantage of new biomedical technologies.”

Rasgon contributed to the panel regarding strategies available to prevent, treat, and control malaria, including diagnostics, drugs, vaccines, and vector control. The panel discussed the need to use available resources more effectively and to strategically develop new intervention strategies.

“We have made amazing progress in our ability to treat and control malaria,” said Rasgon, “but eradicating it completely remains a challenge. During the panel, we discussed strategies to combine new and existing approaches to maximize their effectiveness and to prevent the rebound of malaria in areas where it has been eliminated.”

In addition to Llinás and Rasgon, individuals from over 15 research labs at Penn State, including those at Penn State Milton S. Hershey Medical Center and Penn State York, focus their research on some aspect of malaria and regularly meet through the Huck Institutes of the Life Sciences Center for Malaria Research (CMaR), with Llinás acting as a Co-Director. The Center serves to encourage its members to leverage the diverse approaches to malaria research at Penn State and to forge new collaborations.

[ G L M ]

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]]>No publisherglm173biochemistry and molecular biologyresearchMain page news2018-01-08T17:00:08Z2018/01/08 09:25:00 US/EasternNews ItemAgricultural parasite takes control of host plant’s geneshttp://science.psu.edu/news-and-events/2018-news/Axtell1-2018 Dodder, a parasitic plant that causes major damage to crops in the U.S. and worldwide every year, can silence the expression of genes in the host plants from which it obtains water and nutrients.

Dodder, a parasitic plant, attached to a host plant from which it obtains water and nutrients. The parasite inserts microRNAs into the host that can silence the expression of host genes. This is the first example of cross-species gene regulation observed in a parasitic plant. CREDIT: Penn State University

Dodder, a parasitic plant that causes major damage to crops in the U.S. and worldwide every year, can silence the expression of genes in the host plants from which it obtains water and nutrients. This cross-species gene regulation, which includes genes that contribute to the host plant’s defense against parasites, has never before been seen from a parasitic plant. Understanding this system could provide researchers with a method to engineer plants to be resistant to the parasite. A paper describing the research by a team that includes scientists at Penn State and Virginia Tech appears January 4, 2018 in the journal Nature.

“Dodder is an obligate parasite, meaning that it can’t live on its own,” said Michael J. Axtell, professor of biology at Penn State and an author of the paper. “Unlike most plants that get energy through photosynthesis, dodder siphons off water and nutrients from other plants by connecting itself to the host vascular system using structures called haustoria. We were able to show that, in addition to the nutrients that flow into dodder from the host plant across the haustoria, dodder passes microRNAs into its host plant that regulate the expression of host genes in a very direct way.”

MicroRNAs are very short bits of nucleic acid -- the material of DNA and RNA -- that can bind to messenger RNAs that code for protein. This binding of microRNA to messenger RNA prevents the protein from being made, either by blocking the process directly or by triggering other proteins that cut the messenger RNA into smaller pieces. Importantly, the small remnants of the messenger RNA can then function like additional microRNAs, binding to other copies of the messenger RNA, causing further gene silencing.

“Dodder seems to turn on the expression of these microRNAs when it comes into contact with the host plant,” said James H. Westwood, professor of plant pathology, physiology, and weed science at Virginia Tech and another author of the paper. “What was really interesting is that the microRNAs specifically target host genes that are involved in the plant’s defense against the parasite.”

When a plant is attacked by a parasite it initiates a number of defense mechanisms. In one of these mechanisms, similar to blood clotting after a cut, the plants produce a protein that clots the flow of nutrients to the site of the parasite. MicroRNA from dodder targets the messenger RNA that codes for this protein, which then helps to maintain a free flow of nutrients to the parasite. The gene that codes for this clotting protein has a very similar sequence across many plant species, and the researchers showed that the microRNA from dodder targets regions of the gene sequence that are the most highly conserved across plants. Because of this, dodder can probably silence this clotting protein in, and therefore parasitize, a wide variety of plant species.

The researchers sequenced all of the microRNAs in tissue from the parasite alone, the host plant alone, and a combination of two. By comparing the sequencing data from these three sources, they were able to identify microRNAs from dodder that had entered the plant tissue. They then measured the amount of messenger RNA of genes that were targeted by the dodder microRNAs and saw that the level of messenger RNA from the host was reduced when the dodder microRNAs were present.

“Along with previous examples of small RNA exchange between fungi and plants, our results imply that this cross-species gene regulation may be more widespread in other plant-parasite interactions,” said Axtell. “So, with this knowledge, the dream is that we could eventually use gene editing technology to edit the microRNA target sites in the host plants, preventing the microRNAs from binding and silencing these genes. Engineering resistance to the parasite in this way could reduce the economic impact of the parasite on crop plants.”

In addition to Axtell and Westwood, the research team includes Saima Shahid, Nathan R. Johnson, Eric Wafula, Feng Wang, Ceyda Coruh, and Claude W. dePamphilis at Penn State; Gunjune Kim and Vivian Bernal-Galeano at Virginia Tech; and Tamia Phifer at Knox College. The research was funded by the U.S. National Science Foundation and the U.S. National Institute of Food and Agriculture. Additional support was provided by the Penn State Huck Institutes of the Life Sciences.

[ Sam Sholtis ]

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]]>No publishersjs144biologyresearchMain page news2018-01-03T18:05:06Z2018/01/03 13:05:6.967504 US/EasternNews ItemFour-dimensional physics in two dimensionshttp://science.psu.edu/news-and-events/2018-news/Rechtsman1-2018 For the first time, physicists have built a two-dimensional experimental system that allows them to study the physical properties of materials that were theorized to exist only in four-dimensional space.

Illustration of light passing through a two-dimensional waveguide array. Each waveguide is essentially a tube, which behaves like a wire for light, inscribed through high-quality glass using a powerful laser. Many of these waveguides are inscribed closely spaced through a single piece of glass to form the array. Light that flows through the device behaves precisely according to the predictions of the four-dimensional quantum Hall effect. CREDIT: Rechtsman laboratory, Penn State University

For the first time, physicists have built a two-dimensional experimental system that allows them to study the physical properties of materials that were theorized to exist only in four-dimensional space. An international team of researchers from Penn State, ETH Zurich in Switzerland, the University of Pittsburgh, and the Holon Institute of Technology in Israel have demonstrated that the behavior of particles of light can be made to match predictions about the four-dimensional version of the “quantum Hall effect” -- a phenomenon that has been at the root of three Nobel Prizes in physics -- in a two-dimensional array of “waveguides.”

A paper describing the research appears January 4, 2018 in the journal Nature along with a paper from a separate group from Germany that shows that a similar mechanism can be used to make a gas of ultracold atoms exhibit four-dimensional quantum Hall physics as well.

“When it was theorized that the quantum Hall effect could be observed in four-dimensional space,” said Mikael Rechtsman, assistant professor of physics and an author of the paper, “it was considered to be of purely theoretical interest because the real world consists of only three spatial dimensions; it was more or less a curiosity. But, we have now shown that four-dimensional quantum Hall physics can be emulated using photons -- particles of light -- flowing through an intricately structured piece of glass -- a waveguide array.”

When electric charge is sandwiched between two surfaces, the charge behaves effectively like a two-dimensional material. When that material is cooled down to near absolute-zero temperature and subjected to a strong magnetic field, the amount that it can conduct becomes “quantized” -- fixed to a fundamental constant of nature and cannot change. “Quantization is striking because even if the material is ‘messy’ -- that is, it has a lot of defects -- this ‘Hall conductance’ remains exceedingly stable,” said Rechtsman. “This robustness of electron flow -- the quantum Hall effect -- is universal and can be observed in many different materials under very different conditions.”

This quantization of conductance, first described in two-dimensions, cannot be observed in an ordinary three-dimensional material, but in 2000, it was shown theoretically that a similar quantization could be observed in four spatial dimensions. To model this four-dimensional space, the researchers built waveguide arrays. Each waveguide is essentially a tube, which behaves like a wire for light. This “tube” is inscribed through high-quality glass using a powerful laser.

Many of these waveguides are inscribed closely spaced through a single piece of glass to form the array. The researchers used a recently-developed technique to encode “synthetic dimensions” into the positions of the waveguides. In other words, the complex patterns of the waveguide positions act as a manifestation of the higher-dimensional coordinates. By encoding two extra synthetic dimensions into the complex geometric structure of the waveguides, the researchers were able to model the two-dimensional system as having a total of four spatial dimensions. The researchers then measured how light flowed through the device and found that it behaved precisely according to the predictions of the four-dimensional quantum Hall effect.

“Our observations, taken together with the observations using ultracold atoms, provide the first demonstration of higher-dimensional quantum Hall physics,” said Rechtsman. “But how can understanding and probing higher-dimensional physics have some relevance to science and technology in our three-dimensional world? There are a number of examples where this is the case. For example, ‘quasicrystals’ -- metallic alloys that are crystalline but have no repeating units and are used to coat some non-stick pans -- have been shown to have ‘hidden dimensions:’ their structures can be understood as projections from higher-dimensional space into the real, three-dimensional world. Furthermore, it is possible that higher-dimensional physics could be used as a design principle for novel photonic devices.”

In addition to Rechtsman, the research team includes Jonathan Guglielmon at Penn State; Oded Zilberberg at ETH Zurich; Sheng Huang, Mohan Wang, and Kevin Chen at the University of Pittsburgh; and Yaacov E. Kraus at the Holon Institute of Technology. The research was supported by the U.S. National Science Foundation, the Charles E. Kaufman Foundation, the Alfred P. Sloan Foundation, and the Swiss National Science Foundation.

[ Sam Sholtis ]

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]]>No publishersjs144researchphysicsMain page news2018-01-03T18:02:27Z2018/01/03 13:02:27.295931 US/EasternNews ItemAlien Megastructure not the cause of dimming of the 'Most Mysterious Star in the Universe'http://science.psu.edu/news-and-events/2018-news/alien-megastructure-not-the-cause-of-dimming-of-the-most-mysterious-star-in-the-universe A team of more than 200 researchers, including Penn State Department of Astronomy and Astrophysics Assistant Professor Jason Wright and led by Louisiana State University's Tabetha Boyajian, is one step closer to solving the mystery behind the "most mysterious star in the universe."

This illustration depicts an uneven ring of dust orbiting KIC 8462852, also known as Boyajian’s Star or Tabby's Star.
Credit: NASA/JPL-Caltech

A team of more than 200 researchers, including Penn State Department of Astronomy and Astrophysics Assistant Professor Jason Wright and led by Louisiana State University's Tabetha Boyajian, is one step closer to solving the mystery behind the "most mysterious star in the universe." KIC 8462852, or "Tabby's Star," nicknamed after Boyajian, is otherwise an ordinary star, about 50 percent bigger and 1,000 degrees hotter than the Sun, and about 1,000 light years away. However, it has been inexplicably dimming and brightening sporadically like no other. Several theories abound to explain the star's unusual light patterns, including that an alien megastructure is orbiting the star.

The mystery of Tabby's Star is so compelling that more than 1,700 people donated over $100,000 through a Kickstarter campaign in support of dedicated ground-based telescope time to observe and gather more data on the star through a network of telescopes around the world. As a result, a body of data collected by Boyajian and colleagues in partnership with the Las Cumbres Observatory is now available in a new paper in The Astrophysical Journal Letters.

"We were hoping that once we finally caught a dip happening in real time we could see if the dips were the same depth at all wavelengths. If they were nearly the same, this would suggest that the cause was something opaque, like an orbiting disk, planet, or star, or even large structures in space" said Wright, who is a co-author of the paper, titled "The First Post-Kepler Brightness Dips of KIC 8462852." Instead, the team found that the star got much dimmer at some wavelengths than at others.

"Dust is most likely the reason why the star's light appears to dim and brighten. The new data shows that different colors of light are being blocked at different intensities. Therefore, whatever is passing between us and the star is not opaque, as would be expected from a planet or alien megastructure," Boyajian said.

The scientists closely observed the star through the Las Cumbres Observatory from March 2016 to December 2017. Beginning in May 2017 there were four distinct episodes when the star's light dipped. Supporters from the crowdfunding campaign nominated and voted to name these episodes. The first two dips were named Elsie and Celeste. The last two were named after ancient lost cities -- Scotland's Scara Brae and Cambodia's Angkor. The authors write that in many ways what is happening with the star is like these lost cities.

"They're ancient; we are watching things that happened more than 1,000 years ago," the authors wrote. "They're almost certainly caused by something ordinary, at least on a cosmic scale. And yet that makes them more interesting, not less. But most of all, they're mysterious."

The method in which this star is being studied -- by gathering and analyzing a flood of data from a single target -- signals a new era of astronomy. Citizen scientists sifting through massive amounts of data from the NASA Kepler mission were the ones to detect the star's unusual behavior in the first place. The main objective of the Kepler mission was to find planets, which it does by detecting the periodic dimming made from a planet moving in front of a star, and hence blocking out a tiny bit of starlight. The online citizen science group Planet Hunters was established so that volunteers could help to classify light curves from the Kepler mission and to search for such planets.

"If it wasn't for people with an unbiased look on our universe, this unusual star would have been overlooked," Boyajian said. "Again, without the public support for this dedicated observing run, we would not have this large amount of data."

Now there are more answers to be found. "This latest research rules out alien megastructures, but it raises the plausibility of other phenomena being behind the dimming," Wright said. "There are models involving circumstellar material -- like exocomets, which were Boyajian's team's original hypothesis -- which seem to be consistent with the data we have." Wright also points out that "some astronomers favor the idea that nothing is blocking the star -- that it just gets dimmer on its own -- and this also is consistent with this summer's data."

Boyajian said, "It's exciting. I am so appreciative of all of the people who have contributed to this in the past year -- the citizen scientists and professional astronomers. It's quite humbling to have all of these people contributing in various ways to help figure it out."

]]>No publishersws139astronomy and astrophysicsresearchMain page news2018-01-10T16:46:05Z2018/01/03 10:40:00 US/EasternNews ItemUnderstanding enzyme cascades key to understanding metabolismhttp://science.psu.edu/news-and-events/2017-news/Sen12-2017 Breaking down sugars create a gradient of chemicals in the body, providing an environment where intracellular complexes might form. This new research may lead to a better understanding of human metabolism.

Like ants, one enzyme follows the trail left behind by the previous one. In this case, the initial substrate is acted upon by enzyme A, leaving a substrate suitable for enzyme B and on down the line. Credit: Ayusman Sen

A spoonful of sugar may make the medicine go down, but understanding what happens to that sugar in the cell is far more complicated than simple digestion, according to researchers.

For sugars to metabolize and provide energy to the cells, a series of enzymes – biological catalysts – must each, in turn, break down a reactant. In this case, the researchers used glucose, the sugar found in corn syrup and one of the two sugars that result when table sugar – sucrose – is broken down in the body.

In this cascade, the first enzyme acts on the glucose supplied to the cell, and the subsequent enzymes work on successive products. In the process, two adenosine triphosphate molecules –ATP – are consumed but four are produced. The hydrolysis of ATP powers many cellular processes to maintain the cell's viability. Similar enzyme cascades are responsible for many metabolic processes in the body.

Enzymes that participate in such reaction pathways have in some cases been shown to form intracellular, reversible complexes termed metabolons by Paul Srere (deceased), University of Texas Southwestern Medical School. Having the enzymes in proximity to one another facilitates the series of reactions they catalyze. One such example is the purinosome discovered in Stephan J. Benkovic's Lab at Penn State that consists of six enzymes involved in the biosynthesis of purines.

The researchers asked whether one of the factors contributing to metabolon formation could be a gradient of chemicals generated by the participating enzymes. They report their results in the December 18, 2017 issue of Nature Chemistry.

"We discovered some time ago that simple catalyst molecules such as enzymes will also chemotax up the gradient of a reactant," said Ayusman Sen, Distinguished Professor of Chemistry, Penn State. "They move toward higher and higher concentrations of reactant."

The movement is termed chemotaxis, where individual molecules migrate along a concentration gradient of other molecules.

"All living things chemotax," said Sen. "If you are hungry and suddenly smell French fries, you will try to walk toward the fries. If the smell decreases, you will randomly turn to try to find the higher concentration of French fry odor molecules until you are at the French fry counter."

In their study, the researchers used only the first four enzymes of the glycolytic pathway — hexokinase, phosphoglucose isomerase, phosphofructokinase and aldolase. These four steps actually consume ATP. To study the movement of the enzymes, the researchers used fluorescent tagging of hexokinase and aldolase, the first and fourth enzymes in the pathway. Each was tagged with a different fluorescent dye so the movement of both enzymes could be followed.

They looked at three cases -- the normal reaction where hexokinase phosphorylates glucose; the reaction of hexokinase with mannose, a sugar that binds more strongly but has a slower reaction rate; and finally with L-glucose, a form of glucose that is not used by hexokinase. The phosphorylation requires ATP. In the presence of phosphoglucose isomerase – the second enzyme --and phosphofructokinase – the third enzyme-- the reactant for aldolase is produced.

The researchers observed that the aldolase moves towards the hexokinase in their flow experiment, revealing that aldolase was chemotaxing up the reactant gradient produced by the functioning of the first three enzymes in the pathway. The chemotaxis was greatest with D-glucose, less with mannose and not observed with L-glucose.

Theoretical modeling of the enzyme movement qualitatively predicted the extent of enzyme movement.

The researchers also looked at whether chemotaxis of enzymes would occur in a model of the exceptionally crowded intracellular environment. They added a large molecular weight substance to simulate such crowding. Chemotaxis still occurred, but at a slower rate.

"Chemotaxis along a chemical gradient could be a factor in assembly of enzyme clusters such as metabolons," said Benkovic, Evan Pugh University Professor and Eberly Chair in Chemistry, Penn State. "Other factors, such as noncovalent interactions would still be expected to contribute."

The resolution of the research instrument, however, was insufficient to demonstrate in this case that the four enzymes were assembling into a metabolon. The researchers observed the formation of large aggregates of enzymes, but could not demonstrate they were functioning metabolons.

Also working in this project from Penn State are first author Xi Zhao, graduate student in chemistry; Michelle M. Spiering, assistant research professor of chemistry; and Peter J. Butler professor of biomedical engineering. Vinita Yadav, a recent doctoral recipient now at the Dow Chemical Company was also on the team. Others on the team were Henri Palacei and Henry Hess, Department of Biomedical Engineering, Columbia University and Michael Gilson, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego.

The National Science Foundation and the Defense Threat Reduction Agency supported this work.

[ A'ndrea Elyse Messer ]

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]]>No publisherglm173chemistryresearchMain page news2017-12-18T16:29:16Z2017/12/18 11:30:00 US/EasternNews ItemTurning pathogens against each other to prevent drug resistancehttp://science.psu.edu/news-and-events/2017-news/Read12-2017 Limiting a much-needed resource could pit pathogens against one another and prevent the emergence of drug resistance.
Click on the image for a high-resolution version. CREDIT: Penn State.

Limiting a much-needed resource could pit pathogens against one another and prevent the emergence of drug resistance. New research demonstrates that harnessing competition among pathogens inside a patient could extend the life of existing drugs where resistance is already present and prevent resistance to new drugs from emerging. A paper describing this ecological approach to drug resistance appears the week of December 11, 2017 in the journal Proceedings of the National Academy of Sciences.

“Drug resistance is hindering efforts to control HIV, tuberculosis, and malaria, which collectively kill nearly 3 million people worldwide every year,” said Nina Wale, graduate student at Penn State at the time of the research and lead author of the paper. “It also complicates recovery from major surgeries and cancer chemotherapy. We are faced with a big problem: what can we do when a patient is infected with a drug-resistant pathogen, which will cause treatment to fail? We could use other drugs, but other drugs may not be available and developing new ones is a lengthy and expensive process. By taking advantage of competition between parasites inside a host, we managed to use an existing drug to successfully treat an infection, even when drug-resistant parasites were already there.”

Drug resistance originates when a pathogen -- such as a parasite, virus, or bacterium --develops a genetic mutation that allows it to avoid being killed by the drug. Even if only one individual pathogen has this mutation, as is frequently the case when resistance first arises, that one individual can replicate into a population of billions once it survives drug treatment. But resistance often comes with a cost, and drug-resistant pathogens often do not acquire certain resources as efficiently as other pathogens, or they may require more of the resource.

“In the absence of drug treatment, the only thing that stops resistant pathogens from spreading is competition with the pathogens that are sensitive to drug treatment,” said Andrew Read, Evan Pugh Professor of Biology and Entomology and Eberly Professor of Biotechnology at Penn State and senior author of the paper. “We’re utilizing the natural force of competition to control the resistant ones and using conventional drugs to treat the sensitive ones.”

Strategic limitation of resources increases competition among pathogens within a patient. This intervention combined with traditional drugs that might otherwise fail can successfully treat an infection, as illustrated in this animation. Credit: Penn State

The researchers manipulated a nutrient in the drinking water of mice that is used by malaria parasites during an infection -- just as a gardener might manipulate nutrients through fertilizers to favor certain plants. This dietary intervention was used alongside traditional drugs as a sort of combination therapy.

“We treated mice infected with drug-sensitive malaria parasites with traditional drugs,” said Wale. “When mice were given the nutrient, the treatment failed in 40 percent of the mice, and we confirmed by a variety of tests that this was because drug-resistant strains had popped up. But when the nutrient was limited, the infection did not rebound in a single mouse. So by limiting this nutrient, we prevented the emergence of drug resistance.”

The researchers then confirmed that their results were due to competition among parasites and not some other effect of limiting the nutrient. When drug-treated mice were infected only with resistant strains and the nutrient was limited, the resistant parasites survived. But when drug-treated mice were infected with both sensitive and resistant parasites, limiting the nutrient stopped resistant parasites from growing at all -- even when resistant parasites were initially present at far greater numbers than when they typically first appear in a host.

“This study is a proof-of-principle that an ecological manipulation can make it possible to continue using a drug,” said Read, “even when resistant pathogens that would otherwise cause a treatment failure are present at great numbers. People have already been looking for weak points of resistant pathogens, but they do it in the absence of susceptible ones. Our work shows that studies that do not involve this competition aspect are missing the natural force that keeps resistance under control, and that is missing a huge amount of potential for manipulation.”

This work suggests a new direction of study that would allow researchers to capitalize on the natural competition between pathogens to control the emergence of drug resistance. For infections like tuberculosis and malaria, where drug-resistant strains to traditional drugs already exist, researchers must next identify a resource or nutrient for which drug-resistant strains have greater needs than sensitive strains; confirm that limiting the resource would lead to the elimination of resistant strains; determine the most effective intervention strategy to remove the resource; and pinpoint the ideal timing of the intervention. For an infection where a new drug is being developed, these questions could be addressed during the drug development phase.

“Researchers already go to great lengths to identify drug resistance as a routine part of drug development,” said Read. “You could work the development of a resource-limiting intervention into that drug development pipeline. The initial cost would increase, but after that relatively small initial investment, you might be able to extend the lifetime of a drug. It costs a hundred million dollars or more to bring a new drug to market, so the payoff could be quite big.

“Typically if a physician detects drug resistance in an infection, they won’t use that drug. And that’s okay if you’ve got another option. But if you haven’t got another option, this is the sort of manipulation that would allow you to treat the patient even when resistance is there.”

In addition to Wale and Read, the research team includes Derek Sim, Matthew Jones, and Rahel Salathe at Penn State and Troy Day at Queen’s University in Kingston, Ontario. This work was funded by the Institute of General Medical Science.

[ Gail McCormick ]

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]]>No publisherglm173biologyresearchMain page news2017-12-12T17:50:20Z2017/12/11 15:00:00 US/EasternNews ItemMathematical model mimics melanomahttp://science.psu.edu/news-and-events/2017-news/Suhov11-2018 Cancer cells’ ability to tolerate crowded conditions may be one key to understanding tumor growth and formation, according to a mathematical model that has been applied to cancer cell growth for the first time.

Mathematical model mimics melanoma. Left: melanoma cells grown in culture with normal cells form clusters that resemble proto-tumors. Right: Simulations using a modified version of the Widom-Rowlinson model replicate patterns of melanoma cell growth seen in laboratory experiments by controlling the exclusion area -- the amount of space required -- around two types of simulated cells as they grow and spread. Credit: Penn State

Cancer cells’ ability to tolerate crowded conditions may be one key to understanding tumor growth and formation, according to a mathematical model that has been applied to cancer cell growth for the first time. The model can replicate patterns of melanoma cell growth seen in laboratory experiments by controlling the ‘exclusion area’ -- the amount of space required -- around two types of simulated cells as they grow and spread. A paper describing the model and experiments appears in a recent issue of the journal Scientific Reports.

“When our collaborators grew melanoma cancer cells in a mixed culture with normal cells,” said Yuri Suhov, professor of mathematics at Penn State and an author of the paper, “the cancer cells grew and spread more quickly, forming clusters of melanoma cells surrounded by non-cancer cells. This clustered pattern of melanoma cells resembled two-dimensional proto-tumors, so we were interested in modeling this pattern formation in order to understand what about the cancer cells allows them to grow in this way. Melanoma is a skin cancer of a relatively rare occurrence. However, it is one of most lethal forms of cancer characterized by a high potential for metastasis, which makes it crucial to understand the dynamics of the tumor growth and develop methods for early detection.”

The researchers applied a modification of the Widom-Rowlinson model -- a mathematical model that has been used in contexts ranging from theoretical chemistry to sociology -- to try to determine what factors explained the pattern of cell growth seen in the laboratory experiments. Their model simulates the growth of two cell types that initially are evenly mixed and evenly spaced across a grid. By varying parameters of the model, the researchers can control the rate at which each cell type replicates, dies, and migrates, as well as the required exclusion area around the cells.

“By altering the exclusion distance between the two cell types in the simulations, we were able to replicate the clustered patterns seen in the experiments,” said Izabella Stuhl, visiting assistant professor in mathematics at Penn State and another author of the paper. “The cell type with the narrower exclusion area was more tolerant of dense conditions and formed patterns almost identical to the clusters of melanoma cells seen in the laboratory experiments. This suggests that a reduction in ‘contact inhibition’ -- a known factor that stops cells from replicating when they bump into other cells -- may be what allows tumors to form.”

Simulated cancer cells (black) grow and form clusters surrounded by non-cancer cells (yellow) replicating experimental results. The simulations, based on a modification of the Widom-Rowlinson model, may give researchers clues to the factors that allow tumors to form. Credit: Penn State

In the course of their work, the researchers first made predictions based on the mathematical model. Then numerical simulations were conducted, in parallel with the co-culture experiments. The simulated results were repeatedly compared with the experimental data.

The researchers plan to continue to expand their model in combination with data from real-world experiments in cancer cell growth. This combination of theoretical modeling with laboratory experiments could lead to additional insights into the factors that contribute to cancer cell growth.

“Tumors grow in places where normal, healthy cells can’t because the cells are already densely packed,” said Suhov. “Contact inhibition, which we modeled as exclusion area, may be one of the things that prevents non-cancer cells from spreading uncontrollably, but cancer cells somehow overcome this. On the other hand, the normal cells try to form ‘border layers’, of a higher cell density, surrounding tumor-like clusters as if they wanted to isolate tumors and prevent them from spreading further. Our model shows that these factors are relevant when one tries to explain the images of cell growth seen in the laboratory. It is quite remarkable that the mixture of cells from unrelated biological sources shows a persistent pattern of behavior. However, we would like to expand this to gain a better understanding of how cancer cells behave within a natural setting. As we continue to refine our model based on additional experimental data, we may be able to build in parameters that allow us to better understand the precise biological processes that cause tumors to form.”

In addition to Suhov and Stuhl, the research team included Mauro César Cafundó Morais, Alan U. Sabino, Willian W. Lautenschlager, Alexandre S. Queiroga, Tharcisio Citrangulo Tortelli Jr., Roger Chammas, and Alexandre F. Ramos. The research was supported by the Coordenao de Aperfeioamento de Pessoal de Nível Superior (CAPES) in Brazil, the University of Denver Department of Mathematics, the Programa de Educação - MEC/SESu in Brazil, and the Penn State Department of Mathematics.

[ Sam Sholtis ]

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]]>No publishersjs144mathematicsresearchMain page news2017-11-30T15:34:46Z2017/11/30 10:35:00 US/EasternNews ItemFlies' disease-carrying potential may be greater than thought, researchers sayhttp://science.psu.edu/news-and-events/2017-news/flies-disease-carrying-potential-may-be-greater-than-thought-researchers-say A new study adds further proof to the suspicion that houseflies and blowflies carry and spread a variety of species of bacteria that are harmful to humans.Flies can be more than pesky picnic crashers, they may be potent pathogen carriers, too, according to an international team of researchers.

In a study of the microbiomes of 116 houseflies and blowflies from three different continents, researchers found, in some cases, these flies carried hundreds of different species of bacteria, many of which are harmful to humans. Because flies often live close to humans, scientists have long suspected they played a role in carrying and spreading diseases, but this study, which was originally initiated at Penn State's Eberly College of Science, adds further proof, as well as insights into the extent of that threat.

"We believe that this may show a mechanism for pathogen transmission that has been overlooked by public health officials, and flies may contribute to the rapid transmission of pathogens in outbreak situations,” said Donald Bryant, Ernest C. Pollard Professor of Biotechnology and professor of biochemistry and molecular biology, Penn State.

According to Stephan Schuster, former professor of biochemistry and molecular biology, Penn State, and now research director at Nanyang Technological University, Singapore, the researchers were able to investigate the microbial content of individual fly body parts, including legs and wings. The legs appear to transfer most of the microbial organisms from one surface to another, he added.

"The legs and wings show the highest microbial diversity in the fly body, suggesting that bacteria use the flies as airborne shuttles," said Schuster. "It may be that bacteria survive their journey, growing and spreading on a new surface. In fact, the study shows that each step of hundreds that a fly has taken leaves behind a microbial colony track, if the new surface supports bacterial growth."

Researchers used a scan electron microscope to find where bacterial cells and particles attach to the fly body. The electron microscope captures an up close look at the head of a blowfly in this picture. Image credit: Ana Junqueira and Stephan Schuster.

Blowflies and houseflies — both carrion fly species — are often exposed to unhygienic matter because they use feces and decaying organic matter to nurture their young, where they could pick up bacteria that could act as pathogens to humans, plants and animals. The study also indicates that blowflies and houseflies share over 50 percent of their microbiome, a mixture of host-related microorganisms and those acquired from the environments they inhabit. Surprisingly, flies collected from stables carried fewer pathogens than those collected from urban environments.

The researchers, who report their findings in the current issue of Scientific Reports, found 15 instances of the human pathogen Helicobacter pylori, a pathogen often causing ulcers in the human gut, largely in the blowfly samples collected in Brazil. The known route of transmission of Helicobacter has never considered flies as a possible vector for the disease, said Schuster.

The potential, then, for flies to carry diseases may increase when more people are present.

"It will really make you think twice about eating that potato salad that’s been sitting out at your next picnic," Bryant said. "It might be better to have that picnic in the woods, far away from urban environments, not a central park."

Ana Carolina Junqueira, professor of genetics and genomics at the Federal University of Rio De Janeiro and previous postdoctoral fellow at the Singapore Centre for Environmental Life Sciences Engineering (SCELSE), said that the novel genomic and computational methods used for the study allowed the team an unprecedented look at the microbial community carried by flies.

"This is the first study that depicts the entire microbial DNA content of insect vectors using unbiased methods," Junqueira said. "Blowflies and houseflies are considered major mechanical vectors worldwide, but their full potential for microbial transmission was never analyzed comprehensively using modern molecular techniques and deep DNA sequencing."

Flies may not be all bad, however. The researchers suggest they could turn into helpers for human society, perhaps even serving as living drones that can act as an early-warning system for diseases.

"For one, the environmental sequencing of flies may use the insects as proxies that can inform on the microbial content of any given environment that otherwise would be hard or impossible to sample," said Schuster. "In fact, the flies could be intentionally released as autonomous bionic drones into even the smallest spaces and crevices and, upon being recaptured, inform about any biotic material they have encountered."

The Singapore Ministry of Education, the Singapore Center for Environmental Life Sciences Engineering, and the United Nations supported this work.

Bryant, Schuster and Junqueira also worked with Aakrosh Ratan, assistant professor, Center for Public Health Genomics, University of Virginia; Enzo Acerbi, research fellow, Daniela I. Drautz-Moses, senior research fellow, Balakrishnan N.V. Premkrishnan, research associate, and Rikky W. Purbojati, ‎research assistant, all of the Singapore Centre for Environmental Life Sciences Engineering, Nanyang Technological University; Nicolas E. Gaultier, research associate, and Paul I. Costea, postdoctoral fellow, both of the European Molecular Biology Laboratory; Bodo Linz, assistant professor of veterinary medicine, University of Georgia; Ana Maria L. Azeredo-Espin, professor of genetics, evolution and bioagents, and Daniel F. Paulo, doctoral student in molecular biology and genetic engineering, both of State University of Campinas; Poorani Subramanian, computational biology specialist, University of Maryland, and Nur A. Hasan, vice president of research and development, CosmosID Inc. and adjunct associate professor in bioinformatics and computational biology, both of University of Maryland; Rita R. Colwell, founder, CosmosID Inc. and Distinguished University Professor in the Institute for Advanced Computer Studies, University of Maryland and Johns Hopkins Bloomberg School of Public Health; and Peer Bork, group leader, senior scientists and head of Structural and Computational Biology, European Molecular Biology Unit.